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Progression of ocular sulfur mustard injury: development of a model system
Author(s) -
Milhorn Denise,
Hamilton Tracey,
Nelson Marian,
McNutt Patrick
Publication year - 2010
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2010.05491.x
Subject(s) - sulfur mustard , proinflammatory cytokine , medicine , inflammation , pathology , necrosis , cornea , immunology , ophthalmology , toxicity
Exposure of tissues to sulfur mustard (SM) results in the formation of protein and nucleotide adducts that disrupt cellular metabolism and cause cell death. Subsequent pathologies involve a significant proinflammatory response, disrupted healing, and long‐term defects in tissue architecture. Following ocular exposure, acute corneal sequelae include epithelial erosions, necrosis, and corneal inflammation. Longer term, a progressive injury becomes distributed throughout the anterior chamber, which ultimately causes a profound remodeling of corneal tissues. In many cases, debilitating and vision‐threatening injuries reoccur months to years after the initial exposure. Preliminary data in humans suffering from chronic epithelial lesions suggest that thymosin β4 (Tβ4) may be a viable candidate to mitigate acute or long‐term ocular SM injury. To evaluate therapeutic candidates, we have developed a rabbit ocular exposure model system. In this paper, we report molecular, histological, ultrastructural, and clinical consequences of rabbit ocular SM injury, which can be used to assess Tβ4 efficacy, including timepoints at which Tβ4 will be assessed for therapeutic utility.